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Hydrocortisone (HC) injection in rabbits induced eosinopoenia (reduction in absolute eosinophil count) which could be successfully abolished by beta--adrenoceptor antagonists, a propranolol, sotalol, practolol and H 35/25 but not by alpha--adrenoceptor antagonist, phenoxybenzamine. Reserpine per se produced eosinopoenia followed by eosinophilia. However, reserpine pretreatment failed to abolish HC-induced eosinopoenia. It is suggested that the eosinopoenia is mediated through beta--adrenoceptors, which could not be differentiated into beta 1/beta 2--adrenoceptor subtypes as has been possible for other beta-adrenoceptor mediated responses.

Interaction of insulin with beta-adrenoceptor antagonists was studied in conscious rabbits. Propranolol and metoprolol did not modify the peak of insulin hypoglycaemia but delayed its recovery. Practolol, sotalol and 1-INPEA enhanced the peak effect and delayed the recovery of insulin-induced hypoglycaemia. H 35/25 and d-INPEA did not modify insulin hypoglycaemia. The beta-blockers did not produce significant hypoglycaemia per se. Since sotalol, 1-INPEA (specific beta-adrenoceptor antagonists devoid of local anaesthetic activity); practolol and metoprolol (selective cardiac beta-1 adrenoceptor antagonists) enhanced hypoglycaemic action of insulin and H 35/25 (a selective beta-2 adrenoceptor antagonist) failed to affect it, it seems that selective beta-adrenoceptor blockade (similar to cardiac beta-1 adrenoceptors) mediates enhancement of insulin hypoglycaemia. Caution should, therefore, be exercised in administering beta-adrenoceptor antagonists and insulin together. A reduction in the dose of insulin may be necessary.

The study was undertaken to evaluate a new method of estimating plasma fibrinogen levels, gravimetrically using calcium chloride in albino rats. The results were compared with the standard method in which thrombin was used as clotting agent and were found to be statistically not significant. Advantages of using calcium chloride instead of thrombin have been discussed.

Albino rats were pretreated orally for seven days with different doses of the essential oil and juice of garlic. These animals were challenged with isoprenaline (85 mg/kg, s.c.) on day six and seven to induce myocardial necrosis. The same rats were also subjected to swimming test before and after forty eight hr of first injection of isoprenaline. Pretreatment with essential oil (2.0 and 4.0 mg/kg) and juice (2.0 and 4.0 ml/kg) significantly protected the myocardium from isoprenaline-induced necrosis. These animals also exhibited better swimming performance. In separate group of animals, pretreatment with garlic juice (4.0 ml/kg) or essential oil (4.0 mg/kg) improved the chances of survival in isoprenaline-challenged animals.